TLC in Bronchial asthma

[Afina91]

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Why don't TLC in BA (normal compliance, increased resistance, same transairway pressure) decrease (instead stays normal) due to decreased radius of airways (Boyle's law)?

 

[Gurby]

due to decreased radius of airways (Boyle's law)?

Why do we care about Boyle's law here? Isn't Poiseuille's law more relevant? Q = pi*r^4 / 8nl

Flow will be lower with the narrowed airways, but if we increase pressure or increase duration of the breath we can still reach the same lung volume.

 

[NotYou20]

In acute asthma, tlc is increased. Air it's obstructed from getting out in all obstructive lung diseases= higher residual volume= higher tlc. This is to do with bronchioles collapsing during expiration. When you inhale, the pressure in your thorax is negative, meaning transpulmonary pressure is positive. There's more pressure inside the bronchioles than outside so they stay open. During expiration, transpulmonary pressure becomes negative in everyone. Small airways physiologically collapse before all air is exhaled. Hence, residual volume. In asthma, this happens much earlier than it does in a healthy person= higher residual volume= increased total lung capacity.

 

[Gurby]

In acute asthma, tlc is increased. Air it's obstructed from getting out in all obstructive lung diseases= higher residual volume= higher tlc. This is to do with bronchioles collapsing during expiration. When you inhale, the pressure in your thorax is negative, meaning transpulmonary pressure is positive. There's more pressure inside the bronchioles than outside so they stay open. During expiration, transpulmonary pressure becomes negative in everyone. Small airways physiologically collapse before all air is exhaled. Hence, residual volume. In asthma, this happens much earlier than it does in a healthy person= higher residual volume= increased total lung capacity.

Would think that simply increasing residual volume shouldn't increase TLC, but it looks like you are right! My mind has been blown at least once per day since we started respiratory physiology.

http://www.atsjournals.org/doi/full/10.1513/pats.200808-091RM

There is a well-known, and somewhat variable, rise of TLC in asthma (43, 44), but the mechanism of this rise still remains poorly understood. However, a clue to the mechanism underlying this phenomenon comes from, of all places, observations in competitive breath-hold divers (45, 46). A technique known as volume packing used by these divers to increase breath-hold times is associated with a profound increase (1 L) in TLC and an increase in static elastic recoil pressures of greater than 80 cm H2O! Eventually, as lung volume increases, a mechanism to prevent over-distention of the chest wall must be activated, likely involving strong inhibitory reflexes from the respiratory muscles. Alternatively, this postulated reflex is not active during an exacerbation, thus allowing the TLC to rise until the maximum limit of chest deformation is reached. Up until this maximal deformation point is reached, TLC increases in direct proportion to the degree of airway closure that occurs.; hence chest wall hyperinflation defends the FVC and in turn the FEV1 (46). Once the limit of chest wall expansion has been reached, however, further increases in RV due to lung decruitment will result in falls in both FVC and FEV1